I have a strong feeling that Covid-19 is going to be with us for a long time.
The problem with that is with a lot of the vulnerable population. This isn't "the flu".
The problem with that is with a lot of the vulnerable population. This isn't "the flu".
In fact, the 4 other endemic coronaviruses in the human population with zoonotic origin can be traced via mutational drift to their leap to humans; the most recent I believe came from cattle in the 1800s.
These other coronaviruses are mostly a problem only for immunocompromised individuals such as transplant recipients.
The real issue IMO is whether SARS-CoV-2 was artificially engineered (ok, even if it weren’t it is more like SARS and MERS) and whether it will remain potently virulent even for healthy individuals who are exposed as children (as we all were to the endemic coronaviruses).
The fact that most VOCs popped in areas with little to no vaccination coverage quite aligns with that.
For omicron the main hypothesis is it actually evolved in a severely immunocompromised HIV patient.
Edit:
This isn't exactly new[0] and it's also been witnessed for SARS-CoV-2[1]:
> These compilations of case reports indicate the need to identify whether certain forms of immunosuppression are associated with an increased risk of such multimutational escape patterns — for instance, specific cancers or specific therapies, such as the development of B-cell aplasia related to CAR T-cell or anti-CD20 therapy, prolonged use of glucocorticoids, long-term chemotherapy, or radiotherapy. Similarly, organ transplant recipients and those with untreated or poorly controlled human immunodeficiency virus infection may also have prolonged SARS-CoV-2 infection and could constitute a reservoir of divergent escape variants that can spread in the general community. Prolonged viral replication in the context of an inadequate immune response facilitates the emergence of immune-pressure escape mutations.[0]
I'd appreciate an actual counter argument, other than a poorly understood Marek disease analogy.
* Hiding this fact is a serious problem of the 'never name a mutation by a place' new WHO policy.
Considering that even the most highly vaccinated places on earth are shattering records of infection rates, it seems implausible that vaccinating the rest of the world would somehow fix this issue. The "most unvaccinated" places on earth are also some of the most populous, therefore a variant is most likely to arise there out of pure chance.
In this case, due to the large number of mutations, the prime suspect is an untreated HIV patient with a lingering infection, which is most likely to happen in the southern parts of Africa. It's not clear whether vaccines prevent lingering infection in such a case.
OP was suggesting intentionally limiting vaccination. If 'natural' immunity can also allow for antibody-evading mutations, than we get nothing from limiting vaccinations - my point exactly.
>Considering that even the most highly vaccinated places on earth are shattering records of infection rates, it seems implausible that vaccinating the rest of the world would somehow fix this issue.
We cannot make mutation never happen, but we can limit the damage by vaccinating more. This will help us gain time to get more effective medications.
No, that doesn't follow. Vaccines target a spike protein specifically, hence selecting for a variant that defeats that particular kind of immunity, making vaccines obsolete for those that need them the most. This is a hypothetical vaccine-escape variant, not this Omicron variant. We know nothing about its actual capability for vaccine-escape.
Natural immunity targets the whole virus, so whatever immune-escape such a virus evolves, it would have to be far more comprehensive to have a significant effect. We may or may not have that in this particular variant and we're still at the very beginning of that wave:
https://pbs.twimg.com/media/FFGNLl3XMAsNQXE?format=jpg&name=...
A virus avoiding spike antibodies would have an advantage whether these antibodies were 'natural' or not, so it's far from clear natural immunity wouldn't lead to the same mutations - all the VOCs hail from mostly unvaxed countries, which leads to the suspicion that it does.
Sure, the 'naturally immune' sick people having extra N-targeting antibodies would be in an advantage vs the virus, but the cost of that is having a real corona infection earlier on, with all the risk simply being frontloaded.
* EDIT: the Chinese vaccines are inactivated virus vaccines. One wonders whether they fare better or worse vs this variant. Then again, maybe this variant will fail to transmit effectively and will just kill itself off like Beta did.
> Sure, the 'naturally immune' sick people having extra N-targeting antibodies would be in an advantage vs the virus, but the cost of that is having a real corona infection earlier on, with all the risk simply being frontloaded.
It's not a binary, when people get vaccinated and then infected (or vice versa), they do develop broader immunity. Frontloading the risk of infection versus vaccination may well be justified in the young and healthy population, but that opinion has been ostracized from the mainstream.
> the Chinese vaccines are inactivated virus vaccines. One wonders whether they fare better or worse vs this variant.
Not all of them are, but CoronaVac is. This[1] suggests that while efficacy of CoronVac against wild-type infection was modest (51%), the reduction when confronted with Gamma was very small (49.6%).
> Then again, maybe this variant will fail to transmit effectively and will just kill itself off like Beta did.
Beta didn't "kill itself off", it led to wave that rivaled Delta/Gamma in some cases. It ended up being outcompeted by Delta/Gamma.
[1] https://www.who.int/news-room/feature-stories/detail/the-sin...
There isn't. We have to theorize on the move, so to speak.
>Frontloading the risk of infection versus vaccination may well be justified in the young and healthy population, but that opinion has been ostracized from the mainstream.
The problem is that people took the wrong assumptions when calculating the risk of disease. All our calculations of risk are based on hospital treatment being available: providing Oxygen, Dexamethasone and ECMO treatment to critically ill patients, and no extra deaths due to healthcare overload.
No scenario when we 'let it rip' involves being able to give Oxygen to all young people who need it, and there will be extra deaths due to overload. The clever people suggesting intentional infection assumed risk factors dependent on current policies without understanding that under their policies risk would shoot up.
>Beta didn't "kill itself off", it led to wave that rivaled Delta/Gamma in some cases. It ended up being outcompeted by Delta/Gamma.
That's functionally equivalent to 'killing itself off', or at least being much less of a threat. I recall Beta's transmission factor was lower than Alpha? Was it because it missed some key mutations, or because mutating to avoid immunity came with a cost?
This is highly speculative. Considering the exposure and infection rates among the younger population, particularly those of school age, can't we say we did let it rip? Infection seroprevalence in blood-donors was at 20% by July[1]. How much worse could it possibly be?
https://jamanetwork.com/journals/jama/fullarticle/2784013?al...
(Ominous music)
>Infection seroprevalence in blood-donors was at 20% by July[1]
Seriously though, two points:
A) I have doubts about this measurement - that level (83.3% with antibodies!) should have been enough for herd immunity in May 2021, yet we don't see it in the US, cases being broadly static in the last month*.
Perhaps American blood donors are highly nonrepresentative even after demographic adjustments? Or they're catching people with very low levels of antibodies but without true immunity? The paper is thorough regarding geographic and demographic factors, but isn't very clear on the technical details of the measurement itself beyond 'we did it, here are the results'.
Or we could argue the US had herd immunity in May yet lost it two months after, that's not very encouraging, not even for 'natural' immunity.
B) Assuming the researchers are correct, that's 20% for over a year. That's very different from having it way quicker.
>can't we say we did let it rip?
School closures, remote learning, masks even at that age. Obviously there have been (arguably way overzealous) efforts at controlling COVID even at the youngest ages.
* There's a very recent fall, it's probably reporting lag - or it's really down, but per the research that should have already happened long ago.
The 83% includes immunity from vaccination which, as we know now, is not sufficient for herd immunity. Natural immunity may not be sufficient either.
> School closures, remote learning, masks even at that age. Obviously there have been (arguably way overzealous) efforts at controlling COVID even at the youngest ages.
In many cases, schools didn't get closed during much of the Delta wave and incidence in the young population was particularly high. As for masks: They have a modest effect at best (20% risk reduction).
I never thought about it that way. That would mean, if the virus evolves a more efficient ACE-2 binding domain that the mRNA vaccines fail to recognize, the vaccinated population would be more at risk than the unvaccinated population who has been previously exposed.
"Geneticists and infectious disease specialists there have uncovered potentially dangerous coronavirus mutations in a 36-year-old woman with uncontrolled HIV who was unable to shake the SARS-CoV-2 virus for close to eight months."
That was reported back in June:
https://www.latimes.com/science/story/2021-06-03/why-reachin...
[2] https://www.ft.com/content/06334a7b-30cc-40bf-942b-e3bcd2efb...
[0] https://www.theguardian.com/world/2021/nov/26/vaccine-resist... [EDIT]
SARS2 mutates much more slowly than Influenza so, IMO, we actually NEED to get people more infected. I would not be saying this if we locked every country down in the beginning but this is where we are.
The overall evolutionary path for the virus is most likely to be in the direction of higher infectivity and lower deadliness. Viruses don't tend to replicate in dead hosts, so, a virus that doesn't kill people is fitter evolutionarily than one which does. This means that, while the virus is certainly not going away, the risk eventually will.
This may take a long time, though. It may take decades.
Here is an article from New Scientist that says essentially the same thing, but in more detail: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7825868/
Edit: Fixed typos
o DNA is really complex to work with; designing proteins is harder when you don't have the luxury of being Nature itself and trying it out in vivo.
o You will have a PR problem of hilarious proportions. Virus genetic engineering research labs are a few points short of popular support at the moment.
Both are safe, but in the oral one the virus can go to another person and cause no problems, and then to another and cause no problems, and after like a year jumping hosts it can mutate and become dangerous. Now most of the the polio cases are caused by virus that mutated from the version of the vaccine. https://en.wikipedia.org/wiki/Polio_vaccine#Vaccine-induced_...
The number is much smaller that the number of cases before the vaccine, but it's concerning anyway. So they are trying to discontinue the use of the vaccine with the inactivated virus, but the other one is better when most of the population is not vaccinated. https://en.wikipedia.org/wiki/Polio_vaccine#Schedule
So ... probably the authorization and test necessaries to use a new vaccine with and attenuated virus are more difficult than a vaccine with an inactivated virus (or a vector virus, of mRNA, that also can't spread).
* So they are trying to discontinue the use of the vaccine with the weakened virus, but the it's better when most of the population is not vaccinated.
This make me feel that spreading it is better than not spreading it at this point. Luckily it is much more infectious.
Any lung infection will have a lasting effect (in survivors).
In lucky cases, pneumonia is caused by bacteria sensitive to antibiotics. If it's viral (flu, SARS/MERS/SARS-Cov-2 or anything else) or antibiotic resistant hospital bactery, that's basically it.
At the same time, COVID is also significantly more dangerous than Influenza for the older age groups. The two diseases are very different, but we still need to compare them to get an understanding of the actual dangers. We've always lived with the danger of communicable diseases. It's never going away. If we constantly bombard people with the risks of this particular disease, it will cause a lot of stress and anxiety, which is significantly associated with all-cause mortality.
[1] https://freopp.org/comparing-the-risk-of-death-from-covid-19...
The article you link does not claim that long term impairment is frequent. From the article:
> A UK study estimates that between 7% and 18% of people who had COVID-19 went on to develop some symptoms of long COVID that lingered for at least 5 weeks.
However, this study does not consider severity of symptoms. Someone with a persistent cough for 5 weeks after infection is considered to have “long COVID,” just as someone with massive loss of pulmonary function is considered to have “long COVID.” It also does not control for long COVID symptoms that are merely correlatory, e.g. insomnia. I had intermittent insomnia for the first few months of the pandemic, because I was afraid for the state of the world. Yet if I had contracted COVID in those months, I too could be considered a long COVID sufferer.
I have yet to see a study that estimates the prevalence of severe long-term symptoms causally stemming from COVID infections. My guess is that it’s vanishingly small; given the sheer number of COVID infections, it would be obvious to everyone if a sizable portion of them actually went on to develop severe long-term symptoms. If 7-18% of COVID infections actually resulted in the severe long COVID symptoms described in the article (e.g. “extreme fatigue, breathlessness, [or] difficulty concentrating”), it would be extremely evident on a societal level.
You do not have relevant acquaintances to confirm that anecdotally - numbers aside, as a real risk?
> it would be extremely evident on a societal level
For the cognitive aspect, I am not sure it could become so evident, given the already suboptimal situation. (If you live in a place where "all are bright", please let me know what that encouraging utopia is: I will relocate within the month.) This is not sarcasm or even irony: I believe that cognitive issues are ignored in many societies, and/hence a further decline will hardly be visible. Again, a few in my circle have noted that, but they just go on working as before. This friend of mine had an accident years ago, and started losing his "laser-like precision": he mentioned his concern with the director, who replied «You are simply getting older». I believe that the consideration of relative cognitive falls is very normally relegated to either passing episodes or normal ageing as revealed in natural jerks.
That seems like a weak counter-argument. If this was the case we'd be hearing, and reading, about it everywhere.
The poster was referring to post infection "long covid", and stated suspect that the number of actual cases of "infection caused consequences" could be small. Before, in priority, challenging that idea, the poster was asked whether he actually met acquaintances who were "normal" before infection, and claiming being dramatically hit many months after. This is to pose a preliminary point about the existence of the problem, before considering the magnitude - one black swan entails black swans exist. That was the scope. So, not really an argument (to the poster's full point).
> If this was the case we'd be hearing, and reading, about it everywhere
Hearing, it depends who you hear; reading, I think mention of long covid can be found with reasonable frequency. I submitted one of the divulgative articles in mid October ( https://news.ycombinator.com/item?id=28854321 ). Progress in the development of information leaves could "always" be faster and better.
>The mean (SD) age of survivors was 54.4 (8.9) years, 140 196 (56%) were male, and 197 777 (79%) were hospitalized during acute COVID-19
I would expect the prevalence of severe long-term symptoms to be much higher in a population that was predominantly hospitalized for acute COVID than in the general population. I could not find any stratification by age/risk group/vaccination status from a cursory look at the study, although maybe it’s buried somewhere.
I still have yet to see a study that assesses, given full vaccination, the risk of developing severe long-term symptoms for different risk groups (e.g. ages/comorbidities). This is the most relevant metric for easing restrictions, since acute symptoms for vaccinated individuals have already been shown to be on par with a flu. If chronic symptoms are nonexistent, then there’s no reason to not totally ease restrictions amongst highly vaccinated populations.
https://www.newscientist.com/article/mg25033403-400-long-cov...